Nitric oxide neurotoxicity in neurodegenerative diseases

被引:129
作者
Boje, KMK [1 ]
机构
[1] SUNY Buffalo, Dept Pharmaceut Sci, Sch Pharm & Pharmaceut Sci, Buffalo, NY 14260 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2004年 / 9卷
关键词
nitric oxide; blood brain barrier; neuroinflammation; neurodegenerative diseases; Acquired Immune Deficiency Syndrome (AIDS) dementia complex; HIV-Associated Dementia; amyotrophic lateral sclerosis; Alzheimer's Disease; Huntington's Disease; multiple sclerosis; Parkinson's Disease; review;
D O I
10.2741/1268
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nitric oxide (nitrogen monoxide; NO) is a simple molecule with diverse biological functions. NO and related reactive nitrogen oxide species (RNOS) mediate intricate physiological and pathophysiological effects in the central nervous system. Depending on environmental conditions, NO and RNOS can initiate and mediate neuroprotection or neurotoxicity either exclusively or synergistically with other effectors. The focus of this review is limited to the neuroprotectant/neurotoxic role of NO in Acquired Immune Deficiency Syndrome (AIDS) Dementia Complex (aka HIV-Associated Dementia; HAD) Amyotrophic Lateral Sclerosis (aka Lou Gehrig's Disease), Alzheimer's Disease, Huntington's Disease, Multiple Sclerosis and Parkinson's Disease. This review will shed light on the question: "How important is NO in neurodegenerative diseases?"
引用
收藏
页码:763 / 776
页数:14
相关论文
共 167 条
[1]   Mechanisms and structural determinants of HIV-1 coat protein, gp41-induced neurotoxicity [J].
Adamson, DC ;
Kopnisky, KL ;
Dawson, TM ;
Dawson, VL .
JOURNAL OF NEUROSCIENCE, 1999, 19 (01) :64-71
[2]   Immunologic NO synthase: Elevation in severe AIDS dementia and induction by HIV-1 gp41 [J].
Adamson, DC ;
Wildemann, B ;
Sasaki, M ;
Glass, JD ;
McArthur, JC ;
Christov, VI ;
Dawson, TM ;
Dawson, VL .
SCIENCE, 1996, 274 (5294) :1917-1921
[3]   Rate and severity of HIV-associated dementia (HAD): Correlations with Gp41 and iNOS [J].
Adamson, DC ;
McArthur, JC ;
Dawson, TM ;
Dawson, VL .
MOLECULAR MEDICINE, 1999, 5 (02) :98-109
[4]  
Agerman K, 1999, ANN NY ACAD SCI, V884, P131
[5]  
Aizenman E, 1998, PROG BRAIN RES, V118, P53
[6]   Analysis of the cytosolic proteome in a cell culture model of familial amyotrophic lateral sclerosis reveals alterations to the proteasome, antioxidant defenses, and nitric oxide synthetic pathways [J].
Allen, S ;
Heath, PR ;
Kirby, J ;
Wharton, SB ;
Cookson, MR ;
Menzies, FM ;
Banks, RE ;
Shaw, PJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (08) :6371-6383
[7]   Inducible nitric oxide synthase up-regulation in a transgenic mouse model of familial amyotrophic lateral sclerosis [J].
Almer, G ;
Vukosavic, S ;
Romero, N ;
Przedborski, S .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (06) :2415-2425
[8]  
Almer G, 2001, ANN NEUROL, V49, P176, DOI 10.1002/1531-8249(20010201)49:2<176::AID-ANA37>3.3.CO
[9]  
2-O
[10]   Oxidative signalling and inflammatory pathways in Alzheimer's disease [J].
Anderson, I ;
Adinolfi, C ;
Doctrow, S ;
Huffman, K ;
Joy, KA ;
Malfroy, B ;
Soden, P ;
Rupniak, HT ;
Barnes, JC .
NEURONAL SIGNAL TRANSDUCTION AND ALZHEIMER'S DISEASE, 2001, 67 :141-149